Atherothrombosis as a systemic disease.

Atherothrombosis is a generalized disease process that affects large- and medium-diameter arteries throughout the arterial tree. The trigger of the ischaemic clinical events is the complication of a disrupted atherosclerotic plaque by the formation of a platelet-rich thrombus. These thrombotic events are not always clinically manifest; in most cases, the thrombotic reaction remains parietal but contributes to plaque growth by infiltration of the thrombus by smooth muscle cells. In addition, the evolution of the thrombotic reaction destroys the microvasculature of the downstream tissue by subclinical platelet thrombi. Less often, the resulting thrombus leads to partial or total occlusion of the affected artery with subsequent ischaemic clinical manifestations such as ischaemic stroke, unstable angina and Q-wave or non-Q-wave myocardial infarction. The proportion of ischaemic arterial events that is due to atherothrombosis varies according to the vascular bed in which the event occurs, from a near-total dependency for the lower limbs (intermittent claudication) to less than 50% for cerebrovascular events (ischaemic stroke). Occurrence of an arterial ischaemic event due to atherothrombosis implies that other arterial territories may already be affected by a similar pathological process, even if still clinically silent. Treatment of atherothrombotic patients should include the management of cardiovascular risk factors (which aims at the prevention of incidence, evolution and instability of the plaques) and antiplatelet treatment for the prevention of thrombotic complications. Secondary prevention of an ischaemic event in the index territory will provide primary prevention for other arterial territories that are still clinically silent. The aims of antiplatelet therapy are first to prevent the occurrence of acute ischaemic events through inhibition of platelet thrombus formation and second to protect distal tissues through inhibition of microembolization. Due to the systemic nature of the disease, antiplatelet therapy that has shown a proven consistent benefit across all arterial beds is mandatory for optimal prevention of ischaemic events in atherothrombotic patients. Copyright 2002 S. Karger AG, Basel